Q-omics provides the consensus-scored RALYL profile across patient tissues and cancer cell-line models. RALYL expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, RALYL is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, RALYL protein abundance shows 15,381 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UCEC, KIRC, and GBM as cancer lineages where RALYL shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for RALYL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RALYL survival associations across molecular data types. RALYL RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RALYL RNA expression–survival associations across cancer types. High RALYL expression shows unfavorable associations in UCEC, KIRC and UVM, but favorable associations in UCS, LUAD and DLBC. The UCEC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify UCEC as the clearest survival context for RALYL RNA expression.
This table summarizes RALYL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for RALYL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RALYL shows lower tumor expression in KIRC, KICH, KIRP, COAD, READ and STAD. The KIRC box plot shows higher RALYL RNA expression in normal versus tumor tissue (log2 FC = −3.146, t-test p < 0.001).
This table shows molecular features associated with RALYL in patient tissues and cancer cell lines. In patient samples, RALYL shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, RALYL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
